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Network dysfunction in Alzheimer's disease: does synaptic scaling drive disease progression?


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Small, DH 2008 , 'Network dysfunction in Alzheimer's disease: does synaptic scaling drive disease progression?' , Trends in Molecular Medicine, vol. 14, no. 3 , pp. 103-108 , doi: 10.1016/j.molmed.2007.12.006.

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Accumulation of b-amyloid protein (Ab) in the brain is a
key feature of Alzheimer’s disease (AD). The build-up of
aggregated forms of Ab leads to synaptic loss and to
cognitive dysfunction. Although the pathways controlling
production and aggregation of Ab are well studied,
the mechanisms that drive the spread of neurodegeneration
in the brain are unclear. Here, the idea is presented
that AD progresses as a consequence of synaptic
scaling, a type of neuronal plasticity that helps maintain
synaptic signal strength. Recent studies indicate that
brain-derived neurotrophic factor, tumour necrosis factor-
a and a7 nicotinic acetylcholine receptors (a7
nAChRs) regulate synaptic scaling in the AD brain. It is
suggested that further studies on synaptic scaling in AD
could reveal new targets for therapeutic drug development.

Item Type: Article
Authors/Creators:Small, DH
Journal or Publication Title: Trends in Molecular Medicine
ISSN: 1471-4914
DOI / ID Number: 10.1016/j.molmed.2007.12.006
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